The purpose of these studies is to assess the effects of experimental long term pressure overload induced hypertrophy and failure on myocardial performance, coronary perfusion, and myocardial energy metabolism in both adult and developing conscious dog models. The extent to which limitation of coronary vascular reserve can account for changes in ventricular function in the hypertrophied and failing heart at rest and during periods of cardiovascular stress (i.e., in response to severe, spontaneous exercise, short term coronary artery occlusion and administration of potent coronary vasodilators) will be evaluated. Mongrel dogs will be instrumented with: miniature pressure gauges in the aorta and either the left or right ventricle; ultrasonic crystals for measurement of right or left ventricular segment length shortening and wall thickness, and left ventricular internal diameter; ultrasonic flow transducers and hydraulic occluders on either the right main or left circumflex coronary artery; catheters in the right ventricle, left atrium and aorta; and hydraulic occluders on either the pulmonary artery or thoracic aorta for the production of pressure overload hypertrophy and failure of either the right or left ventricles, respectively. Alterations in the regional distribution of myocardial blood flow, as well as the development of coronary collateral circulation in hypertrophied and failing hearts will be measured by the radioactive microsphere technique. Moreover, changes in coronary flow and myocardial function in the presence of cardiac hypertrophy and failure will be correlated with changes in the concentrations of several proteins and their substrates important in regulating energy metabolism in myocardial cells. The goal of these studies is to establish potential cause-effect relationships between alterations in coronary blood flow, myocardial energy metabolism and ventricular performance with the development of cardiac hypertrophy and failure.